Until recently it has been assumed that extra-pulmonary factors play little or no role in the conversion of angiotensin I to angiotensin II. However, it has been shown that significant conversion can occur within the kidney. Therefore, preliminary experiments were carried out to determine the extent to which myocardial tissue can convert angiotensin I to angiotensin II. The results of these experiments indicate that the heart can indeed convert angiotensin I to angiotensin II. The proposed research has three main objectives: (1) to acquire more information in order to quantify the extent of myocardial conversion of angiotensin I to angiotensin II; (2) to determine the extent to which altering the circulating levels of steroids and sodium can alter myocardial conversion of this decapeptide; (3) determine if the administration of angiotensin I induces the release of myocardial catecholamines.